ArticleMolecular and cellular biology1994
Transcriptional activation by herpes simplex virus type 1 VP16 in vitro and its inhibition by oligopeptides.
Article in Molecular and cellular biology, 1994. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
21 citing papers in PubMed, 35 citations in OpenAlex.
- Function-based mutation-resistant synthetic signaling device activated by HIV-1 proteolysis.ACS synthetic biology · 2015Article
- Interaction of Sox1, Sox2, Sox3 and Oct4 during primary neurogenesis.Developmental biology · 2011Article
- Non-structural proteins of Periplaneta fuliginosa densovirus inhibit cellular gene expression and induce necrosis in Sf9 cell cultures.Virus genes · 2009Article
- Article
- HCF-1 functions as a coactivator for the zinc finger protein Krox20.The Journal of biological chemistry · 2003Article
- A single amino acid substitution in herpes simplex virus type 1 VP16 inhibits binding to the virion host shutoff protein and is incompatible with virus growth.Journal of virology · 2003Article
- Zhangfei: a second cellular protein interacts with herpes simplex virus accessory factor HCF in a manner similar to Luman and VP16.Nucleic acids research · 2000Article
- The novel coactivator C1 (HCF) coordinates multiprotein enhancer formation and mediates transcription activation by GABP.The EMBO journal · 2000Article
- Mutations in host cell factor 1 separate its role in cell proliferation from recruitment of VP16 and LZIP.Molecular and cellular biology · 2000Article
- Crystal structure of the conserved core of the herpes simplex virus transcriptional regulatory protein VP16.Genes & development · 1999Article
- Herpes simplex virus transactivator VP16 discriminates between HCF-1 and a novel family member, HCF-2.Journal of virology · 1999Article
- A trans-acting peptide activates the yeast a1 repressor by raising its DNA-binding affinity.The EMBO journal · 1999Article
- The herpesvirus transactivator VP16 mimics a human basic domain leucine zipper protein, luman, in its interaction with HCF.Journal of virology · 1998Article
- Viral mimicry: common mode of association with HCF by VP16 and the cellular protein LZIP.Genes & development · 1997Article
- The VP16 paradox: herpes simplex virus VP16 contains a long-range activation domain but within the natural multiprotein complex activates only from promoter-proximal positions.Journal of virology · 1997Article
- Tetracycline-controlled transcription in eukaryotes: novel transactivators with graded transactivation potential.Nucleic acids research · 1997Article
- Interdigitated residues within a small region of VP16 interact with Oct-1, HCF, and DNA.Molecular and cellular biology · 1997Article
- Protein interactions in the herpes simplex virus type 1 VP16-induced complex: VP16 peptide inhibition and mutational analysis of host cell factor requirements.Journal of virology · 1997Article
- The bovine herpesvirus alpha gene trans-inducing factor activates transcription by mechanisms different from those of its herpes simplex virus type 1 counterpart VP16.Journal of virology · 1995Article
- Proteins and cis-acting elements associated with transactivation of the varicella-zoster virus (VZV) immediate-early gene 62 promoter by VZV open reading frame 10 protein.Journal of virology · 1995Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
VP16 is a herpes simplex virus (HSV)-encoded transcriptional activator protein that is essential for efficient viral replication and as such may be a target for novel therapeutic agents directed against viral gene expression. We have reconstituted transcriptional activation by VP16 in an in vitro system that is dependent on DNA sequences from HSV immediate-early gene promoters and on protein-protein interactions between VP16 and Oct-1 that are required for VP16 activation in vivo. Activation increased synergistically with the number of TAATGARAT elements (the cis-acting element for VP16 activation in vivo) upstream of the core promoter, and mutations of this element that reduce Oct-1 or VP16 DNA binding reduced transactivation in vitro. A VP16 insertion mutant unable to interact with Oct-1 was inactive, but, surprisingly, a deletion mutant lacking the activation domain was approximately 65% as active as the full-length protein. The activation domains of Oct-1 were necessary for activation in reactions containing the VP16 deletion mutant, and they contributed significantly to activation by full-length VP16. Addition of a GA-rich element present in many HSV immediate-early gene enhancers synergistically stimulated VP16-activated transcription. Finally, oligopeptides that are derived from a region of VP16 thought to contact a cellular factor known as HCF (host cell factor) and that inhibit efficient VP16 binding to the TAATGARAT element also specifically inhibited VP16-activated, but not basal, transcription. Amino acid substitutions in one of these peptides identified three residues that are absolutely required for inhibition and presumably for interaction of VP16 with HCF.
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